Heart failure is a debilitating disease in which abnormal function of the heart leads to inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds cardiac muscle causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat, i.e. to increase the stroke volume. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result, typically in the form of myocardial ischemia or myocardial infarction. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. Often, electrical and mechanical dyssynchronies develop within the heart such that the various chambers of the heart no longer beat in a synchronized manner, degrading overall cardiac function.
A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart, compromised filling or valvular dysfunction leads to build-up of fluids (i.e. congestion) in the lungs and other organs and tissues. The accumulation of fluids in the lungs to heart failure is referred to herein as cardiogenic pulmonary edema (PE). Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs, particularly pulmonary venous pressure. Alternatively, a malfunctioning mitral valve which becomes incompetent (i.e., leaky) may result in mitral valve regurgitation that can produce acute elevation in left atrial pressure during left ventricular contraction with increased propensity to developing PE. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs (i.e. the alveoli). This can cause severe respiratory problems and, if left untreated, can be fatal. Note that noncardiogenic forms of PE can arise due to factors besides heart failure, such as infection. More specifically, noncardiogenic PE can be caused by changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult.
Many patients susceptible to CHF and cardiogenic PE, particularly the elderly, have pacemakers, ICDs, CRT devices or other implantable medical devices implanted therein, or are candidates for such devices. Accordingly, it is desirable to provide techniques for detecting and tracking CHF and cardiogenic PE using such devices. One particularly effective parameter for detecting and tracking CHF is cardiac pressure, particularly left atrial pressure (LAP), i.e. the blood pressure within the left atrium of the patient. Reliable detection of LAP would not only permit the implanted device to track CHF/PE for diagnostic purposes but to also control therapies applied to address CHF/PE such as CRT. In this regard, CRT seeks to normalize asynchronous cardiac electrical activation and the resultant asynchronous contractions by delivering synchronized pacing stimulus to the ventricles using pacemakers, ICDs or CRT devices equipped with biventricular pacing capability. The pacing stimulus is typically synchronized so as to help to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis et al., entitled “Multi-Electrode Apparatus And Method For Treatment Of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer et al., entitled “Apparatus And Method For Reversal Of Myocardial Remodeling With Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann et al., entitled “Method And Apparatus For Maintaining Synchronized Pacing.” Reliable estimates of LAP would also allow the dosing of heart failure medications (such as diuretics) to be properly titrated so as to minimize the number of episodes of acute heart failure decompensation. That is, accurate LAP monitoring can provide for the early identification of incipient HF decompensation and guide the adjustment of vasodilator and diuretic dosing. See, also, Ritzema et al., “Physician-directed patient self-management of left atrial pressure in advanced chronic heart failure,” Circulation 2010;121:1086-1095.
However, LAP is a difficult parameter to detect since it is not clinically appealing to place a blood pressure sensor directly in the left atrium due to the chronic risk of thromboembolic events, as well as risks associated with the trans-septal implant procedure itself. Accordingly, various techniques have been developed for estimating LAP based on other parameters that can be more safely sensed by a pacemaker or ICD. In this regard, some particularly promising techniques have been developed that use electrical impedance signals (or related electrical signals such as admittance) to estimate LAP. For example, impedance signals can be sensed along three sensing vectors that form a triangle in which one of the vertices includes an electrode mounted on a left ventricular (LV) lead. The near-field impedance associated with the electrode mounted on the LV lead may be derived using the various “near-field” based impedance techniques described in U.S. patent application Ser. No. 12/853,130, filed concurrently herewith, of Gutfinger et al., entitled “Near Field-Based Systems and Methods for Assessing Impedance for Use by an Implantable Medical Device,” which is also fully incorporated by reference herein. The sensed near-field impedance associated with an electrode mounted on the LV lead is affected by the blood volume inside the left ventricle, which is in turn reflected by the blood volume and pressure in the left atrium. Accordingly, there is a correlation between the derived near-field impedance associated with the electrode mounted on the LV lead and LAP, which can be exploited to estimate LAP and thereby also detect and/or track CHF and warn of cardiogenic PE.
For LAP estimation techniques based on impedance, admittance or related electrical parameters see: U.S. patent application No. 11/559,235, filed Nov. 13, 2006, of Gutfinger et al., entitled “System and Method for Estimating Cardiac Pressure Using Parameters Derived from Impedance Signals Detected by an Implantable Medical Device”, which is incorporated by reference herein, as well as U.S. patent application Ser. Nos. 11/558,101; 11/557,851; 11/557,870; 11/557,882; and 11/558,088, each entitled “Systems and Methods to Monitor and Treat Heart Failure Conditions.” See, also, U.S. patent application Ser. No. 11/558,194, by Panescu et al., entitled “Closed-Loop Adaptive Adjustment of Pacing Therapy based on Cardiogenic Impedance Signals Detected by an Implantable Medical Device”. Still further, see U.S. patent application Ser. No. 12/109,304, filed Apr. 25, 2008, of Gutfinger et al., entitled “System and Method for Calibrating Cardiac Pressure Measurements Derived from Signals Detected by an Implantable Medical Device”. Still further, see, U.S. patent application Ser. No. 12/712,003, of Gutfinger, filed Feb. 24, 2010, entitled “Device and Method for Adjusting Impedance Based on Posture of a Patient.”
At least some of these documents describe cardiac pressure estimation techniques wherein a linear correlation between LAP and impedance (Z)—or related electrical signals such as admittance (Y) or conductance (G)—is exploited by the implanted device to estimate LAP. Briefly, the electrical signals are measured along sensing vectors passing through the heart of the patient in response to impedance-detection pulses generated by the device. Transformations are used to derive the near-field impedance measurements associated with various electrodes. Suitable conversion factors are determined via linear regression (or other suitable techniques) to relate the particular measured electrical signal parameter to LAP, so that measurements can then be used to estimate LAP. In one particular example, the conversion factors are “slope” and “baseline” values representative of the linear correlation between LAP and electrical parameter values measured in response to the impedance-detection pulses. Slope may also be referred to as “gain.” Baseline may also be referred to as “offset” or bLAP (i.e. baseline LAP.) Thereafter, LAP is estimated using:zLAP=Parameter*Slope+Baselinewherein “Parameter” is the electrical parameter measured in response to the impedance detection pulses and zLAP represents the estimated LAP. Note that for the sake of generality, the term zLAP is used herein to refer to estimated LAP values whether based on actual impedance signals, or any of the related electrical signals such as admittance or conductance.
Although the foregoing techniques are helpful, there remains room for further improvement. One concern with using zLAP estimates is that the presence of acute mitral valve regurgitation (MR) can introduce errors into the LAP estimate. In this regard, if acute MR develops, a sudden increase in actual LAP can occur within the patient without a significant immediate change in impedance (or related parameters such as admittance) from which LAP is estimated. If MR becomes sustained (i.e. chronic), impedance values can start to change but with a lag relative to the rise in actual LAP. When chronic MR acutely resolves, there can be a sudden decrease in LAP without any immediate change in impedance. Impedance eventually changes but again with a lag relative to actual LAP. This phenomenon, which is discussed in greater detail below, can affect the capability of an implantable device to properly estimate LAP based on impedance/admittance within patients subject to acute MR.
Accordingly, it is desirable to provide techniques for estimating LAP estimates that takes into account the presence or absence of acute MR within the patient. It is to this end that the invention is primarily directed.